Type I diabetes mellitus does not alter initial splanchnic glucose extraction or hepatic UDP-glucose flux during enteral glucose administration

Aims/hypothesis. Our aim was to determine whether an alteration in splanchn ic glucose metabolism could contribute to postprandial hyperglycaemia in pe ople with Type I (insulin-dependent) diabetes mellitus. Methods. Splanchnic glucose extraction, hepatic glycogen synthesis and endo genous glucose production were compared in 8 Type I diabetic patients and i n 11 control subjects, Endogenous hormone secretion was inhibited with soma tostatin while insulin (similar to 550 pmol/l) and glucagon (similar to 130 ng/l) concentrations were matched with exogenous hormone infusions. Glucos e containing [3-H-3] glucose was infused into the duodenum at a rate of 20 mu mol . kg(-1) . min(-1). Plasma glucose concentrations were maintained at about 8.5 mmol/l in both groups by means of a separate variable intravenou s glucose infusion. Results. Initial splanchnic glucose uptake, calculated by subtracting the s ystemic rate of appearance of [3-H-3] glucose from the rate of infusion of [3-H-3] glucose into the duodenum, did not differ in the diabetic and non-d iabetic patients (4.1 +/- 0.8 vs 3.0 +/- 1.0 mu mol/kg/ min). In addition, hepatic glycogen synthesis, measured using the acetaminophen glucuronide me thod did not differ (10.7 +/- 2.4 vs 10.1 +/- 2.7 mu mol . kg(-1) . min(-1) ). On the other hand, suppression of endogenous glucose production, measure d by an intravenous infusion of [6,6-H-2(2)] glucose, was greater (p < 0.05 ) in the diabetic than in the non-diabetic subjects (1.7 +/- 1.6 vs 5.8 +/- 1.9 <mu>mol . kg(-1) . min(-1)). Conclusion/interpretation. When glucose, insulin and glucagon concentration s are matched in individuals with relatively good chronic glycaemic control , Type I diabetes does not alter initial splanchnic glucose uptake of enter ally delivered glucose or hepatic glycogen synthesis. Alterations in splanc hnic glucose metabolism are not likely to contribute to postprandial hyperg lycaemia in people with well controlled Type I diabetes.